Search

Background: It is understood that coronary heart disease (CHD) is one cause of heart failure, and many risk factors are common to both entities. Hypercholesterolemia, however, being a well-recognized risk factor for CHD, has an unclear association with incident heart failure., Methods: We evaluated the relations of total and high-density lipoprotein (HDL) cholesterol to incident heart failure and CHD in 10,813 US male physicians (mean age, 68 years). Total and HDL cholesterol were analyzed both as continuous and as categorical (in quartiles) variables., Results: There were 222 incident heart failure cases on follow-up (mean, 6 years). In Cox models, after adjusting for traditional coronary risk factors, 1-SD increase in total cholesterol (36.7 mg/dL) and HDL cholesterol (15.3 mg/dL) was not related to incident heart failure with a hazard ratio and 95% CI of 0.91 (0.79-1.05) for total cholesterol and 0.95 (0.82-1.11) for HDL cholesterol. In categorical models, heart failure risk in second, third, and fourth quartiles of total and HDL cholesterol was statistically not different from those in the lowest quartile; hazard ratios with 95% CI were 0.72 (0.49-1.05), 0.76 (0.52-1.11), 0.73 (0.50-1.09) for total cholesterol, and 0.78 (0.53-1.15), 0.66 (0.43-1.00), and 1.03 (0.69-1.54), for HDL cholesterol. Further adjustment for CHD on follow-up or exclusion of individuals with CHD at baseline did not alter the results. In contrast, high total cholesterol and low HDL cholesterol increased the risk of incident CHD (P < .001)., Conclusion: In healthy males, total and HDL cholesterol levels were not related to incident heart failure.

Background: Left ventricular systolic dysfunction (LVSD) and heart failure (HF) are powerful predictors of poor outcome after acute myocardial infarction (MI). It is not known, however, whether the extent of coronary artery disease (CAD) independently influences cardiovascular (CV) outcomes in these high-risk patients., Methods: In the VALIANT, 14703 patients were randomly assigned to receive either captopril monotherapy, valsartan monotherapy, or a valsartan and captopril combination between 0.5 and 10 days after acute MI complicated by LVSD, HF, or both. Cox proportional hazards models were used to evaluate the relation between the extent of CAD (the number of diseased vessels as assessed by angiography) and a range of CV outcomes and all-cause mortality., Results: Coronary angiography data were available on 5742 (40%) of the 14703 randomized patients. Single-vessel disease was reported in 1955 patients (34%), 2-vessel disease in 1598 (28%), and 3-vessel disease in 2189 (38%). For all CV outcomes, the risk increased with the severity of CAD (P for trend < .002). A comparison of single-, 2-, and 3-vessel disease showed that, after adjusting for all known covariates, including revascularization and ejection fraction, 2-vessel disease was associated with a 40% increased hazard (P = .008) and 3-vessel disease was associated with an 85% increased hazard (P < .001) for all-cause mortality. The fully adjusted hazard ratios for death and other CV outcomes increased significantly with increasing extent of CAD., Conclusions: Increasing extent of CAD, as detected by angiography, is a significant and independent risk factor for adverse CV outcomes after MI complicated by HF, LVSD, or both. The observed risk was apparent even after excluding patients who had undergone revascularization.

Background: Intramyocardial fat deposition occurs as an age-related process and in multiple pathologic processes. Objective: We evaluated the presence of left ventricular (LV) and right ventricular (RV) intramyocardial fat with 64-slice multidetector computed tomography (MDCT). Methods: One hundred persons with no history of coronary artery disease (47 women, 53 men; mean age [± SD], 53 ± 12.2 years) and 25 patients with CT findings of myocardial infarction (17 men, 8 women; mean age, 71.3 ± 9.6 years) were studied for intramyocardial fat in defined segments of the ventricles (17 LV and 10 RV segments) at 3 levels. Fat deposition was defined as density range of −30 to −190 Hounsfield units on images both before and after contrast. Results: In healthy persons, LV intramyocardial fat was primarily located in the basal segments (5% anteroseptal, 5% inferior), and RV intramyocardial fat was primarily located in the anterolateral (24% of base, 23% of mid) and inferolateral (27% base, 27% mid) segments. Older age was associated with an increased odds of RV (sex-adjusted odds ratio [OR] per decade increment, 1.61; 95% confidence interval [CI], 1.11–2.33; P = 0.012) but not LV (OR, 0.97; 95% CI, 0.67–1.40; P = 0.85) intramyocardial fat. Compared with women, men had a lower risk of LV (95% CI, 0.1–0.64; P = 0.004) but not RV (95% CI, 0.35–1.87; P = 0.62) intramyocardial fat. Patients with old myocardial infarction (>3 years) had increased percentage of fat in infarcted left ventricles at all 3 levels (P ≤ 0.004). Conclusions: Intramyocardial fat can be detected by MDCT and is common in healthy and infarcted myocardium. [Copyright &y& Elsevier]

Abstract: Background: Cardiac magnetic resonance imaging (CMR) can accurately determine infarct size. Prior studies using indirect methods to assess infarct size have shown that patients with larger myocardial infarctions have a worse prognosis than those with smaller myocardial infarctions. Objectives: This study assessed the prognostic significance of infarct size determined by CMR. Methods: Cine and contrast CMR were performed in 100 patients with coronary artery disease (CAD) undergoing routine cardiac evaluation. Infarct size was determined by planimetry. We used Cox proportional hazards regression analyses (stepwise forward selection approach) to evaluate the risk of all-cause death associated with traditional cardiovascular risk factors, symptoms of heart failure, medication use, left ventricular ejection fraction, left ventricular mass, angiographic severity of CAD and extent of infarct size determined by CMR. Results: Ninety-one patients had evidence of myocardial infarction by CMR. Mean follow-up was 4.8±1.6 years after CMR, during which time 30 patients died. The significant multivariable predictors of all-cause mortality were extent of myocardial infarction by CMR, extent of left ventricular systolic dysfunction, symptoms of heart failure, and diabetes mellitus (P<.05). The presence of infarct greater than or equal to 24% of left ventricular mass and left ventricular ejection fraction less than or equal to 30% were the most optimal cut-off points for the prediction of death with bivariate adjusted hazard ratios of 2.11 (95% confidence interval 1.02–4.38) and 4.06 (95% confidence interval 1.73–9.54), respectively. Conclusions: The extent of myocardial infarction determined by CMR is an independent predictor of death in patients with CAD. [ABSTRACT FROM AUTHOR]

Current evidence suggests that routine invasive therapy in the setting of unstable angina/non–ST-segment elevation myocardial infarction (UA/NSTEMI) reduces the incidence of composite end points (i.e., death, myocardial infarction, or angina.). The 2002 American College of Cardiology/American Heart Association guidelines recommend invasive therapy in high-risk patients, although it is unknown if such an approach improves survival. We conducted a meta-analysis on 5 studies in 6,766 UA/NSTEMI patients who were randomized to either routine invasive versus conservative therapy in the era of glycoprotein IIb/IIIa inhibitors and intracoronary stents. Compared with conservative therapy, an invasive approach suggested a reduction in mortality at 6 to 12 months (risk ratio [RR] 0.80, 95% confidence interval [CI] 0.63 to 1.03) and at 24 months (RR 0.77, 95% CI 0.60 to 0.99). The composite end point of death or myocardial infarction was reduced throughout all periods of follow-up: at 30 days (RR 0.61, 95% CI 0.45 to 0.84), at 6 months (RR 0.75, 95% CI 0.63 to 0.89), and at 12 months (RR 0.78, 95% CI 0.65 to 0.92). For the same composite end point at 6 to 12 months, men benefited from invasive therapy (RR 0.68, 95% CI 0.57 to 0.81), as did troponin-positive patients (RR 0.74, 95% CI 0.59 to 0.94). The results for women (RR 1.07, 95% CI 0.82 to 1.41) and troponin-negative patients (RR 0.82, 95% CI 0.59 to 1.14) were equivocal. Routine invasive therapy in UA/NSTEMI patients along with adjunctive use of glycoprotein IIb/IIIa inhibitors and intracoronary stents improves survival. Enhanced risk stratification is needed in women and troponin-negative patients so that invasive therapy may be more effectively recommended in these groups. [Copyright &y& Elsevier]